Can coffee help fight both sleepiness and age-related disease? Find out…
Stanford University and University of Bordeaux researchers explored caffeine’s effect on a newly discovered genetic link between chronic inflammation and age-associated disease.
Most of us enjoy coffee or tea to keep us going through the day, but new research suggests that caffeine may also help keep its drinkers going strong later in life.
In a study published in Nature Medicine, researchers report a genetic mechanism responsible for triggering chronic inflammation and the subsequent development of age-related cardiovascular disease. The findings also highlight the role of caffeine consumption in helping disrupt inflammatory gene activity in some older adults.
“Chronic inflammation is a common denominator for almost all diseases of aging, such as hypertension, cancer, and many neurological disorders,” said David Furman, who led the study at Stanford University School of Medicine. “Here, we found that some gene networks that normally participate in response to infections are also those that mediate chronic inflammation during aging. We also learned that caffeine plays an important role here and the effect can be pretty dramatic.”
During an 8-year study, Furman and his team analyzed survey data, blood samples, and medical histories from 100 human participants: a group of adults between ages 20 and 30 and another group of adults over 60 years old.
By comparing gene expression data between the two groups, Furman’s team identified two highly active gene networks in the older age group linked to the production of a powerful inflammatory protein, called IL-1-beta. Of the older age group, nearly half demonstrated high levels of IL-1-beta, as well high levels of nucleic-acid metabolites found to boost inflammatory gene activity and production of IL-1-beta. The team also observed that the metabolites caused systemic inflammation and high blood pressure when injected in mice.
“Most of the participants with high activity in these inflammatory gene networks were also hypertensive or suffering from arterial stiffness,” explained Furman. “Using metabolomics data, we found that one of the metabolites that was high in the inflamed participants was adenosine. In our in vitro studies, caffeine was a big adenosine antagonist, so we asked what their caffeine intake was like.”
The team found that those who were chronically inflamed with high levels of adenine typically did not consume caffeine, while participants with lower levels of inflammation were mostly coffee drinkers, though not all drank coffee.
To further investigate, Furman’s lab incubated immune cells with the metabolites along with caffeine compounds, finding that caffeine blocked the inflammatory effects of the metabolites in the cells.
“The effect was pretty big,” said Furman. “We considered the effect of coffee in milligrams per week, and apparently the effect was linear and surprisingly high for those having 4–5 cups of coffee per day.”
Furman is expanding the team’s study to 1000 participants to explore inflammatory networks that explain other diseases beyond cardiovascular disorders. For now, however, Furman cautions that increasing coffee intake does not by any means guarantee a long life.
“With a sample of 100 people, we cannot really generalize that much, and we need to validate those findings now,” said Furman. “Human biology is complicated, and there are a zillion different pathways that can trigger inflammation…drinking coffee may help in some cases, but things are much more complicated than that.”